Chapter 19Care of Patients with
Pituitary and Adrenal Gland Problems
Disorders of the Anterior Pituitary Gland
Target tissueThyroid, adrenal cortex, ovary, testes, uterus,
mammary glands and kidney
Either excess or deficiency
Pathologic condition within the gland or hypothalmic dysfunction
Two to focus on:HyperpituitarismHypopituitarism
Anterior Pituitary GlandHyper-secretion and or secretion
Pituitary TumorPituitary hyperplasiaBenign adenoma (most common)
Pressure on the optic nerve
Excess GH, ACTH, prolactin (PRL) or TSH
Hypopituitarism Deficiency of one or more anterior pituitary
hormones results in metabolic problems and sexual dysfunction.
Panhypopituitarism—decreased production of all of the anterior pituitary hormones.
Most life-threatening deficiencies—ACTH and TSH.
Deficiency of gonadotropins.
Growth hormoneProportionate dwarfism
Cause of HypopituitarismBenign or malignant tumors
Anorexia nervosa
Shock or severe hypotension
Head trauma
Brain tumors or infection
Congenital
Patient-Centered Collaborative Care
Assessment
Interventions include:Replacement of deficient hormonesAndrogen therapy for virilization; gynecomastia
can occurEstrogens and progesteroneGrowth hormone
Hyperpituitarism Hormone oversecretion occurs with pituitary
tumors or hyperplasia
Genetic considerations
Pituitary adenoma
GigantismGigantism is the onset of growth hormone
hypersecretion before puberty.
AcromegalyGrowth hormone hypersecretion after puberty
Surgical InterventionTranssphenoidal or transfrontal removal of the
pituitary gland
http://www.youtube.com/watch?v=Ebhf1qKVA9A
Patient-Centered Collaborative Care
Assessment
Nonsurgical management:Drug therapy- to reduce GH secretion or the
effects on tissues Somatostatin analoguesDopamine agonistsGrowth hormone antagonist
RadiationGamma knife procedure
Usually one time treatment
Surgical Management
Postoperative Care Monitor neurologic response
Assess for postnasal drip
HOB elevated
Assess nasal drainage
Avoid coughing early after surgery
Assess for meningitis
Hormone replacement
Avoid bending
Avoid strain at stool
Postoperative Care Avoid toothbrushing
Numbness in the area of the incision
Decreased sense of smell
Vasopressin
Diabetes InsipidusWater metabolism problem caused by an
antidiuretic hormone deficiency (either a decrease in ADH synthesis or an inability of the kidneys to respond to ADH)
Diabetes insipidus is classified as:NephrogenicNeurogenic
Patient-Centered Collaborative Care
Assessment
Most manifestations of DI are related to dehydration
Increase in frequency of urination and excessive thirst
Dehydration and hypertonic saline tests used for diagnosis of the disorder
Urine diluted with a low specific gravity (<1.005)
DI: Interventions Oral chlorpropamide
Desmopressin acetate
Early detection of dehydration and maintenance of adequate hydration
Lifelong vasopressin therapy for patients with permanent condition of diabetes insipidus
Teach patients to weigh themselves daily to identify weight gain
Syndrome of Inappropriate Antidiuretic Hormone
Secretion (SIADH)Vasopressin is secreted even when plasma
osmolarity is low or normal.
Feedback mechanisms do not function properly.
Water is retained, resulting in hyponatremia (decreased serum sodium level).
SIADH: Patient-Centered Collaborative Care
Assessment:Recent head traumaCerebrovascular diseaseTuberculosis or other pulmonary diseaseCancerAll past and current drug use
SIADH: InterventionsFluid restriction
Drug therapy—diuretics, hypertonic saline, demeclocycline
Monitor for fluid overload
Safe environment
Neurologic assessment
Adrenal Gland Hypofunction
Adrenocortical steroids may decrease as a result of inadequate secretion of ACTH
Dysfunction of the hypothalamic-pituitary control mechanism
Direct dysfunction of adrenal tissue
Effect of Insufficiency of Adrenocortical Steroids
Loss of aldosterone and cortical action
Decreased gluconeogenesis
Depletion of liver and muscle glycogen
Hypoglycemia
Reduced urea nitrogen excretion
Anorexia and weight loss
Potassium, sodium, and water imbalances
Addison’s DiseasePrimary
Secondary:Sudden cessation of long-term high-dose
glucocorticoid therapy
Acute Adrenal Insufficiency/Addisonian
CrisisLife-threatening event in which the need for
cortisol and aldosterone is greater than the available supply
Usually occurs in a response to a stressful event
Patient-Centered Collaborative Care
Assessment
Clinical manifestations
Assessment Psychosocial assessment
Laboratory tests
Imaging assessment
Adrenal Gland Hyperfunction
Hypersecretion by the adrenal cortex results in Cushing’s syndrome/disease, hypercortisolism, or excessive androgen production
Pheochromocytoma Hyperstimulation of the adrenal medulla caused
by a tumor
Excessive secretion of catecholamines
Hypercortisolism (Cushing’s Disease)
Etiology
Incidence/prevalence
Patient-centered collaborative care
Assessment:Clinical manifestations—skin changes, cardiac
changes, musculoskeletal changes, glucose metabolism, immune changes
Hypercortisolism Cushing’s Disease
Psychosocial assessmentLaboratory tests—blood, salivary and urine cortisol
levels Imaging assessment
Hypercortisolism: Nonsurgical Management
Patient safety
Drug therapy
Nutrition therapy
Monitoring
Hypercortisolism: Surgical Management
Hypophysectomy
Adrenalectomy
Community-Based CareHome care management
Health teaching
Health care resources
Hyperaldosteronism Increased secretion of aldosterone results in
mineralocorticoid excess.
Primary hyperaldosteronism (Conn's syndrome) is a result of excessive secretion of aldosterone from one or both adrenal glands.
Patient-Centered Collaborative Care
Assessment
Most common issues—hypokalemia and elevated blood pressure
Interventions Adrenalectomy
Drug therapy
Glucocorticoid replacement
When surgery cannot be performed—spironolactone therapy
Pheochromocytoma Catecholamine-producing tumors that arise in
the adrenal medulla
Tumors produce, store, and release epinephrine and norepinephrine
Patient-Centered Collaborative Care
Assessment
Interventions:Surgery is main treatment.After surgery, assess blood pressure.